Biomedical subjects
Publications and source records attributed to R F Grossman.
In a family with tuberous sclerosis affecting four generations a mother and daughter had the rare pulmonary manifestations of the disease. Pathologically the pulmonary disease may be the same as pulmonary lymphangioleiomyomatosis.
To assess airway reactivity in lung transplant patients, three heart/lung, three double lung, and eight single lung transplant patients underwent airway challenge tests. All patients were assessed by methacholine aerosol challenge and thirteen were also assessed by histamine aerosol challenge at least three months after transplant surgery. The airways of patients with bilaterally denervated lungs (heart/lung and double lung transplants) were significantly more reactive to both methacholine and histamine (p less than 0.01) than were the airways of patients with unilaterally denervated (single lung transplants) lungs. Inflammatory changes in the airway mucosal biopsies were minimal in three patients and absent in all others. These studies raise questions about the role of central innervation in the maintenance of normal airway function as well as the mechanisms of action of both methacholine and histamine in causing bronchoconstriction.
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We reviewed 17 cases of biopsy-proven sarcoidosis occurring in patients who were 65 years of age or older at the time of diagnosis in order to determine the clinical features of sarcoidosis in this group of elderly patients. A female preponderance (76%) was noted, as well as significant respiratory and cutaneous symptoms. There were no characteristic diagnostic features of sarcoidosis in this group; therefore, we suggest that tissue biopsy is needed to exclude pulmonary diseases such as neoplasm or tuberculosis. Most elderly patients having sarcoidosis remained clinically stable during the period of follow-up and did not require therapy for sarcoidosis. We propose that sarcoidosis should be considered in the differential diagnosis of elderly patients presenting with pulmonary or multisystem disease.
We measured pharyngeal cross-sectional area and its change with alterations in lung volume in 10 subjects who snored and had obstructive sleep apnea, 6 subjects who snored and did not have obstructive sleep apnea, and 9 subjects who did not snore. Pharyngeal area was measured with use of an acoustic-reflection technique. We found that snorers with and without sleep apnea had a significantly smaller mean (+/- SE) pharyngeal cross-sectional area (4.1 +/- 0.2 and 3.7 +/- 0.9 cm2, respectively) at functional residual capacity than nonsnorers (5.4 +/- 0.5 cm2, P less than 0.025). When lung volume decreased from functional residual capacity to residual volume, both nonsnorers and snorers with sleep apnea had a decrease in pharyngeal area (from 5.4 +/- 0.5 to 4.5 +/- 0.4 cm2 and 4.1 +/- 0.2 to 3.4 +/- 0.2 cm2, respectively), whereas snorers without sleep apnea had no such decrease, suggesting that their pharynxes were less collapsible at low lung volumes. We conclude that snorers with and without sleep apnea have smaller pharyngeal cross-sectional areas than nonsnorers and that snorers with sleep apnea have a further decrease as lung volume falls.
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A patient with familial dysautonomia (Riley-Day syndrome) who illustrates the multiple and varied pulmonary manifestations of this disorder is described. Since many of these patients are now surviving well into adulthood, knowledge of this condition among physicians should be propagated.
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The mechanisms responsible for the development of chronic hypercapnia in patients with obstructive sleep apnea (OSA) are not well defined. Therefore, we tested the hypothesis that diffuse airway obstruction may be involved by studying 50 patients with a well-documented OSA syndrome. Seven patients had daytime hypercapnia with a mean PaCO2 of 51 +/- 2 (SEM) mm Hg, compared to a PaCO2 of 35 +/- 1 in the other 43 patients. There were no differences between the 2 groups in the number or duration of nocturnal obstructive events. In contrast, the hypercapnic patients were significantly heavier than the normocapnic patients (body weight, 189 +/- 11 versus 148 +/- 6% of ideal; p less than 0.005) and had evidence of diffuse airway obstruction, as indicated by an increased residual volume and a reduction in all expiratory flow rates. When the hypercapnic patients were compared with a weight-matched group of 9 normocapnic patients (body weight, 196 +/- 8% of ideal), there were still no differences in nocturnal obstructive events, but the differences in tests of airway mechanics persisted. Multiple regression analysis of PaCO2 against several anthropometric, respiratory physiologic, and polysomnographic variables revealed that only 2 variables (expiratory reserve volume and FEV1/FVC), both of which are influenced by airway mechanics, were significantly correlated with PaCO2 (multiple r = 0.78; p = 0.0001). The findings suggest that OSA alone does not produce daytime hypercapnia even in obese patients, and that the presence of diffuse airway obstruction is an important predisposing factor to the development of chronic CO2 retention in such patients.
We report the occurrence of acute pulmonary edema in a patient receiving therapy with nalbuphine, a synthetic narcotic analgesic. Other potential causes of acute pulmonary edema were excluded. It is likely that all opiate drugs share the propensity to produce acute pulmonary edema, and nalbuphine resembles other opiates in this regard.
An 85-year-old woman was brought to the hospital with a serum sodium level of 193 mmol/liter following salt ingestion. She was treated with free water replacement and recovered within 48 hours. She represents the sole survivor of salt ingestion of this severity in the literature.
Among patients with similar degrees of obstructive sleep apnea (OSA) there is considerable variability in the degree of associated nocturnal hypoxemia. The factors responsible for this variability have not been clearly defined. Therefore we studied 44 patients with OSA to identify the physiological determinants of nocturnal arterial O2 saturation (SaO2). All patients underwent pulmonary function testing, arterial blood gas analysis, and overnight polysomnography. Mean nocturnal SaO2 ranged from 96 to 66% and apnea-hypopnea index from 11 to 128 per hour of sleep. Several anthropometric, respiratory physiological, and polysomnographic variables that could be expected to influence nocturnal SaO2 were entered into a stepwise multiple linear regression analysis, with mean nocturnal SaO2 as the dependent variable. Three variables [awake supine arterial PO2 (PaO2), expiratory reserve volume, and percentage of sleep time spent in apnea] were found to correlate strongly with mean nocturnal SaO2 (multiple R, 0.854; P less than 0.0001) and accounted for 73% of its variability among patients. Body weight, other lung volumes, and airflow rates influenced awake PaO2 and expiratory reserve volume but had no independent influence on nocturnal SaO2. In a further group of 15 patients with OSA a high correlation was obtained between measured nocturnal SaO2 and that predicted by the model (r = 0.87; P less than 0.001). We conclude that derangements of pulmonary mechanics and awake PaO2 (generally attributable to obesity and diffuse airway obstruction) are of major importance in establishing the severity of nocturnal hypoxemia in patients with OSA.
Although right heart failure is a recognized complication of obstructive sleep apnea, the incidence and pathogenesis of this complication have not been established. We therefore studied 50 consecutive patients with obstructive sleep apnea to determine the incidence of right heart failure and the factors involved in its development. Six patients (12%) were found to have right heart failure. There were no differences in the number of apneas between those with right heart failure (mean +/- SE, 30 +/- 10 per h sleep) and those without right heart failure (33 +/- 4 per h sleep). In contrast, mean nocturnal oxygen saturation was lower in patients with right heart failure (76 +/- 3%) than in those without right heart failure (90 +/- 1%; p less than 0.001). Furthermore, patients with right heart failure also had a substantially lower awake arterial PO2 (52 +/- 4 mmHg versus 75 +/- 2 mmHg; p less than 0.001) and a higher PCO2 (51 +/- 2 mmHg versus 36 +/- 1 mmHg; p less than 0.001) than those without right heart failure. Severe nocturnal hypoxemia in the absence of diurnal hypoxemia was not associated with right heart failure. Daytime hypoxemia in the patients with right heart failure was associated with a higher residual volume (p less than 0.001) and lower forced expiratory volume in one second (p less than 0.001) than in the patients without right heart failure. The findings suggest that sustained hypoxemia and/or hypercapnia over a 24-h period is a necessary prerequisite for the development of right heart failure in patients with obstructive sleep apnea, and that diffuse airway obstruction plays a major role in causing such hypoxemia.
Diffusing capacity of carbon monoxide (Dco) was measured frequently in a patient with recurrent intrapulmonary hemorrhage secondary to Goodpasture's syndrome. This simple test was found to be a sensitive and useful indicator of the presence or absence of recurrent intrapulmonary hemorrhage. As this is now the major cause of mortality in this disease, we recommended that frequent measurements of the Dco be an important part of its management.
The association between digital clubbing and idiopathic pulmonary fibrosis has been well established; however, the simultaneous occurrence of hypertrophic pulmonary osteoarthropathy and interstitial fibrosis, in the absence of neoplastic disease, has only been described in two case reports and was not mentioned in any of 336 patients described in several recent reviews. Among 70 patients referred for investigation of pulmonary infiltrates, four were found to have hypertrophic pulmonary osteoarthropathy associated with interstitial pulmonary disease, in the absence of malignant disease. We conclude that the use of bone scans and roentgenographic examination of the extremities may draw attention to an association between hypertrophic pulmonary osteoarthropathy and idiopathic pulmonary fibrosis.
We describe a patient who developed fatal bronchiolitis obliterans following gold therapy and review the relationship between rheumatoid arthritis and bronchiolitis.
Pulmonary fat embolism occurs frequently after trauma but its functional significance is often unclear. To obtain direct evidence of lung damage caused by fat embolism we have measured changes in permeability of the alveolar-capillary interface. A permeability index was derived from the half time clearance from lung to blood (T1/2LB) of 99mTcDTPA introduced into the lung in a 1 ml bolus. Three groups of rabbits were studied. Baseline T1/2LB. did not differ significantly between groups. After intravenous injection of saline placebo in one group and of 300 mg/kg triolein in another group there was no change in permeability index. After intravenous injection of 100 mg/kg oleic acid in the third group there was an immediate change in T1/2LB from a monoexponential baseline 280 +/- 20 min (SEM) to a multiexponential curve which was resolved into two components, one with a T1/2LB of 3.2 +/- 0.6 min (SEM) and the other 39.5 +/- 7.6 min (SEM). Statistically significant changes in alveolar-arterial PO2 difference, dynamic compliance, chest radiography, and postmortem lung water accompanied the changes in T1/2LB in this group. There were no significant changes in these variables in the placebo or triolein group. Histological studies of the lung tissue of these animals using the osmic acid stain for fat showed no fat in the placebo group, extensive fat embolisation which was densely stained in the triolein group and much less densely stained fat in the oleic acid group. Measurement of the permeability of the alveolar-capillary interface provides direct evidence of lung damage after oleic acid embolisation. There were no functional changes in animals with extensive embolisation with triolein.
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